Experimental autoimmune uveitis (EAU) is a well established model of human intraocular inflammatory diseases or uveitis and is easily induced in susceptible animal species by immunization with retinal proteins, such as interphotoreceptor retinoid binding protein (IRBP) and S-Antigen (SAg). Marked differences exist among different animal species and strains in their susceptibility to EAU induction but the cause for these differences is not completely clear. Mice are generally resistant to EAU while most rat strains are susceptible. Knowledge about the basic mechanisms underlying resistance to EAU or tolerance induction to ocular proteins may prove beneficial for the treatment or prevention of ocular inflammatory diseases. In FY 1996-1997 we demonstrated that there is strong correlation between constitutive expression of ocular autoantigens in the thymus (mRNA and protein) and resistance to EAU. This correlation was noted both at the species (mice vs. rats or monkeys) and sub-species levels (differences among strains). In 1997-1998 fiscal year we extended these studies to humans and showed that SAg is expressed in human thymi and may therefore serve as a useful indicator of susceptibility to uveitis. Significant effort was directed at testing the general applicability of this concept to other autoimmune diseases. As potential clinical application of this idea will require development of a sensitive assay to quantify levels of thymic expression of putative autoantigens major strides were made towards developing a quantitative in situ PCR assay to meet this need.